ArticleBMC cancer2021
Diallyl thiosulfinate enhanced the anti-cancer activity of dexamethasone in the side population cells of multiple myeloma by promoting miR-127-3p and deactivating the PI3K/AKT signaling pathway.
Article in BMC cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Hidden Activities of Tyrosine Phenol-Lyase and Tryptophan Indole-Lyase: Recombinant PLP-Dependent C-C Lyases as New Biocatalysts for Antimicrobial Thiosulfinate Generation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- The role of antioxidants in multiple myeloma: diagnostic, prognostic, and therapeutic applications: a narrative review.Therapeutic advances in hematology · 2026Review
- Nestin in multiple myeloma: emerging insights into a potential therapeutic target.Frontiers in oncology · 2025Review
- Natural Products and Altered Metabolism in Cancer: Therapeutic Targets and Mechanisms of Action.International journal of molecular sciences · 2024Review
- Curcumin in treatment of hematological cancers: Promises and challenges.Journal of traditional and complementary medicine · 2024Review
- The potential of diallyl trisulfide for cancer prevention and treatment, with mechanism insights.Frontiers in cell and developmental biology · 2024Review
- Prospective Epigenetic Actions of Organo-Sulfur Compounds against Cancer: Perspectives and Molecular Mechanisms.Cancers · 2023Review
- Mechanism of action of Asparagus officinalis extract against multiple myeloma using bioinformatics tools,Frontiers in pharmacology · 2023Article
- Multiple Myeloma Side Population Cells Promote Dexamethasone Resistance of Main Population Cells through Exosome Metastasis of LncRNA SNHG16.Journal of oncology · 2023Article
- Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022Review
- Identification of candidate targets and mechanisms involved in miRNA regulation in multiple myeloma.World journal of surgical oncology · 2022Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSide population (SP) cells, which have similar features to those of cancer stem cells, show resistance to dexamethasone (Dex) treatment. Thus, new drugs that can be used in combination with Dex to reduce the population of SP cells in multiple myeloma (MM) are required. Diallyl thiosulfinate (DATS, allicin), a natural organosulfur compound derived from garlic, has been shown to inhibit the proliferation of SP cells in MM cell lines. Therefore, we investigated the effect of a combination of DATS and Dex (DAT + Dex) on MM SP cells.
methodsSP cells were sorted from MM RPMI-8226 and NCI-H929 cell lines using Hoechst 33342-labeled fluorescence-activated cell sorting. The growth of SP cells was evaluated using the cell counting kit-8 assay. Cell cycle and apoptosis assays were conducted using a BD Calibur flow cytometer. miRNA expression was measured using quantitative reverse transcription-polymerase chain reaction. Phosphoinositide 3-kinase (PI3K), phosphorylated AKT (p-AKT), AKT, p-mechanistic target of rapamycin (mTOR), and mTOR levels were measured using western blot analysis.
resultsOur results showed that the combination of DATS+Dex inhibited sphere formation, colony formation, and proliferation of MM SP cells by inducing apoptosis and cell cycle arrest in the G1/S phase. In addition, the combination of DATS+Dex promoted miR-127-3p expression and inhibited PI3K, p-AKT, and p-mTOR expression in SP cells. Knockdown of miR-127-3p expression weakened the effect of DATS+Dex on cell proliferation, colony formation, apoptosis, and cell cycle of MM SP cells. Additionally, knockdown of miR-127-3p activated the PI3K/AKT/mTOR signaling pathway in MM SP cells cotreated with DATS+Dex.
conclusionWe demonstrated that cotreatment with DATS+Dex reduced cell proliferation, promoted apoptosis, and caused cell cycle arrest of MM SP cells by promoting miR-127-3p expression and deactivating the PI3K/AKT/mTOR signaling pathway.
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